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A 31-year-old female patient with short stature, signs of gonadal dysgenesis, and slight Turner signs is described with a mosaic 45,XO/46,XX del (X) (qter leads to p11) determined with trypsin Giemsa-banding and C-staining [3].

No significant effect on p11 mRNA expression in sigmoid colon or rectum was noted from antidepressant treatment in any of the analyzed subgroups [1].

Two proteins that influence the function of serotonin and serotonergic receptors are serotonin transporter protein (SERT or soluble carrier protein, SLC6A4) and p11 (S-100A10, or calpactin I light chain) [1].

A similar translocation which is however specific for the annexin II2p11(2) complex and early endosomes and does not affect other elements of the cell cortex is observed in cells expressing a trans-dominant annexin II-p11 mutant [7].

The p9 and p11 positivities fused after laminectomy, suggesting that conductance change at the root entry to the bony spinal canal separates these components in the noncephalic reference recording [9].

Description of a pericentric inversion of a chromosome 14 with breakpoints at p11 and q23 leading to duplication-deficiency as a result of crossing over[12].

Combined karyotype and molecular studies on both lymphocytes and fibroblasts allowed correct identification of the abnormality as a complex monosomy/trisomy 21 mosaicism involving a marker derived from idic (21) (p11), and probable assignment of a maternal origin for the error(s) [13].